To serve patients, health care providers, research scientists, scholars, and society by providing excellence and innovation in diagnostic services and educational resources in a respectful, professional and culturally diverse atmosphere.

Our Vision

To become a preeminent leader in academic anatomic and clinical pathology while translating basic science discovery to improved clinical care.

Dr. Steven Carroll is Professor and Chair of the Department of Pathology and Laboratory Medicine and a Research Member of the MUSC Comprehensive Cancer Center’s Cancer Genes and Molecular Regulation Program. Dr. Carroll’s research program, which is funded by NINDS, NCI, the DOD and the Children’s Tumor Foundation, is focused on the mechanisms underlying the pathogenesis of neurofibromatosis type 1-associated peripheral nerve sheath tumors and the development of new therapies for these neoplasms. Dr. Carroll serves as an Associate Editor for the Journal of Neuropathology and Experimental Neurology and has served on the editorial boards of several journals including Neuro-Oncology and The American Journal of Pathology.

Dr. Carroll received his B.S. degree from the University of Memphis in 1981. He then attended Baylor College of Medicine, receiving his Ph.D. in Cell Biology in 1986 and his M.D. in 1988. Dr. Carroll’s postdoctoral research fellowship, Anatomic Pathology Residency and Neuropathology Fellowship were performed at the Washington University School of Medicine (1988-1994). Prior to his arrival at MUSC, Dr. Carroll was Professor of Pathology, Neurobiology and Cell Biology at the University of Alabama at Birmingham (UAB) and the Director of the UAB Division of Neuropathology. While at UAB, Dr. Carroll served as an attending neuropathologist at the University of Alabama Hospital, the Birmingham VA, UAB Highlands Hospital and Alabama Children’s Hospital. He was a Scientist in the UAB Alzheimer’s Disease Research Center, the Mental Retardation Research Center, the Center for Aging, the Center for Glial Biology in Medicine, the Civitan International Research Center and the Center for Neurodegeneration and Experimental Therapeutics as well as being as a Member of the Comprehensive Neuroscience Center and a Senior Scientist in the UAB Comprehensive Cancer Center. Dr. Carroll is certified by the American Board of Pathology in Anatomic Pathology and Neuropathology.

Description
The Carroll laboratory is focused on determining what molecular abnormalities are responsible for the development of schwannomas, plexiform neurofibromas and malignant peripheral nerve sheath tumors (MPNSTs) and using this information to develop effective new treatments for these neoplasms. We have found evidence that abnormal signaling by neuregulin-1 (NRG1), a potent Schwann cell growth factor, promotes the pathogenesis of these peripheral nerve sheath tumors in humans. Based on this evidence, we have developed a novel genetically engineered mouse model in which inappropriate expression of NRG1 in Schwann cells results in the development of large numbers of plexiform neurofibromas. In contrast to previously developed Nf1 knockout mouse models, the plexiform neurofibromas occurring in our genetically engineered mice progress to become MPNSTs at a very high frequency. This animal model thus gives us a unique opportunity to establish both what abnormalities drive the development of plexiform neurofibromas and to determine what subsequent changes cause plexiform neurofibromas to undergo malignant transformation. Using this model and an orthotopic xenograft model we have also developed, we have identified three novel classes of compounds that effectively inhibit the growth of plexiform neurofibromas and MPNSTs in culture and in vivo. To identify additional therapeutic targets in NF-associated peripheral nerve sheath tumors, we are also using NextGen sequencing methods to comprehensively identify all of the genetic changes (mutations) and epigenetic abnormalities driving the development of peripheral nerve sheath tumors; these studies are being performed using tumors collected from human NF patients and tumors developing in our NRG1 overexpressing mouse model. These comprehensive approaches thus continue to identify potential new treatment targets, thereby laying the groundwork for the development of effective new therapies for NF-associated tumors.